Dr Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary, and backstage pass to the journal and its editors. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr Greg Hundley: I'm Greg Hundley, Associate Editor, Director of the Poly Heart Center at VCU Health in Richmond, Virginia. Dr Carolyn Lam: Today's feature discussion is the first huge look at the global, regional and national burden of calcific aortic valve disease and degenerative mitral valve disease over a huge period, from 1990 to 2017. Very important discussion coming right up after this coffee chat. Greg, do you mind if I go first? Dr Greg Hundley: Go ahead, Carolyn. Dr Carolyn Lam: The first paper I want to talk about applies novel single cell transcriptomics to unveil new insights into pressure overload cardiac hypertrophy. Here's your quiz, Greg, ready? Dr Greg Hundley: Well, I'm choking on my coffee here, but go ahead. Dr Carolyn Lam: All right, I was thinking of asking you about single cell transcriptomics but let me just tell you the results. Single cell RNA sequencing is a new and rapidly advancing technique that can comprehensively characterize gene expression and relationships among individual cells. Dr Wang from Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, and Peking Union Medical College and colleagues analyze the transcriptomes of 11,492 single cells and identified major cell types, including both cardiomyocytes and non-cardiomyocytes based on their molecular signatures. They did this at different stages during the progression of pressure overload induced cardiac hypertrophy in a mouse model. Their findings not only illustrated dynamically changing cell type crosstalk doing pathological cardiac hypertrophy, but also shed light on strategies for cell type and stage specific interventions in cardiac disease. For example, subtype switching of macrophages was found to be a key event underlying the transition from normal to decline dejection fraction in cardiac hypertrophy. Thus, targeting macrophages in hypertrophy for example, during the switch could attenuate disease progression. All of this is discussed in an editorial by doctors, Zhang and Zhou from University of Alabama in Birmingham. Dr Greg Hundley: Oh wow. Carolyn very important macrophage infiltration and another role for those, that cell type. Well, my first paper gets at the topic of reversal of these factor Xa inhibitors. In this particular patient population, it's the situation where we're dealing with intracranial hemorrhage. The article comes from Dr G Morgan Jones and colleagues from the University of Tennessee Health Sciences Center. Since the approval of oral factor Xa inhibitors, there have been few papers published really regarding the ability to neutralize the anti-coagulate effects of these agents, particularly after intercranial hemorrhage. Dr Carolyn, this is a multi-center, retrospective, observational cohort study of 433 patients. Then it received apixaban, or rivaroxaban, and then developed an intercranial hemorrhage. They then subsequently received prothrombin complex concentrates in that period of time between 2015 and 2019. Dr Carolyn Lam: Wow. How did these participants who had intracranial hemorrhage, how did they fare after receiving these prothrombin concentrates? Dr Greg Hundley: Yeah, well, administration of the prothrombin complex concentrates after, apixaban or rivaroxaban in the setting of intracranial hemorrhage, provided a high rate of excellent or good hemostasis. That was in nearly 82%, coupled with an adverse consequence of 3.8% of those experiencing a thrombosis. Thrombosis occurred in 25 patients who had a total of 26 thrombotic events of which 22 occurred in the first 14 days, following the prothrombin complex concentrate administration. One patient had documentation of an infusion related reaction. For the full cohort of pati